Fachbereich Veterinärmedizin



    Viral genes and cellular markers associated with neurological complications during herpesvirus infections (2017)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Holz, Carine L
    Nelli, Rahul K
    Wilson, M Eilidh
    Zarski, Lila M
    Azab, Walid (WE 5)
    Baumgardner, Rachel
    Osterrieder, Nikolaus (WE 5)
    Pease, Anthony
    Zhang, Liangliang
    Hession, Sarah
    Goehring, Lutz S
    Hussey, Stephen B
    Soboll Hussey, Gisela
    The journal of general virology; 98(6) — S. 1439–1454
    ISSN: 0022-1317
    DOI: 10.1099/jgv.0.000773
    Pubmed: 28631601
    Institut für Virologie

    Robert-von-Ostertag-Str. 7-13
    Gebäude 35
    14163 Berlin
    Tel. +49 30 838 51833 Fax. +49 30 838 451847

    Abstract / Zusammenfassung

    Despite the importance of neurological disorders associated with herpesviruses, the mechanism by which these viruses influence the central nervous system (CNS) has not been definitively established. Owing to the limitations of studying neuropathogenicity of human herpesviruses in their natural host, many aspects of their pathogenicity and immune response are studied in animal models. Here, we present an important model system that enables studying neuropathogenicity of herpesviruses in the natural host. Equine herpesvirus type 1 (EHV-1) is an alphaherpesvirus that causes a devastating neurological disease (EHV-1 myeloencephalopathy; EHM) in horses. Like other alphaherpesviruses, our understanding of virus neuropathogenicity in the natural host beyond the essential role of viraemia is limited. In particular, information on the role of different viral proteins for virus transfer to the spinal cord endothelium in vivo is lacking. In this study, the contribution of two viral proteins, DNA polymerase (ORF30) and glycoprotein D (gD), to the pathogenicity of EHM was addressed. Furthermore, different cellular immune markers, including alpha-interferon (IFN-α), gamma-interferon (IFN-γ), interleukin-10 (IL-10) and interleukin-1 beta (IL-1β), were identified to play a role during the course of the disease.